Download March 2013 - Hypoglycaemia

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CHEMISTRY LEGEND
MARCH 2013
HYPOGLYCAEMIA
Hypoglycaemia is the medical term for a pathologic state produced by a lower than normal level of blood
glucose. The term hypoglycaemia literally means "under-sweet blood". Hypoglycaemia can produce a variety
of symptoms and effects but the principal problems arise from an inadequate supply of glucose as fuel to the
brain, resulting in impairment of function (neuroglycopenia). Derangements of function can range from
dysphoria or "feeling bad" to coma, seizures, and (rarely) permanent brain damage or death. Hypoglycaemia
can arise from many causes and can occur at any age. It also sometimes occurs at what appears to be random
intervals.
The most common forms of moderate and severe hypoglycaemia occur as a complication of treatment of
diabetes mellitus treated with insulin or less frequently with certain oral medications. Hypoglycaemia is
usually treated by the ingestion or administration of dextrose, or foods quickly digestible to glucose.
The level of glucose low enough to define hypoglycaemia has been a source of controversy in several contexts.
For many purposes, plasma glucose levels below 3.9mmol/L are considered hypoglycaemic.
Defining hypoglycemia
No single glucose value alone serves to define the medical condition termed hypoglycaemia for all people and
purposes. Throughout the 24 hour cycles of eating, digestion, and fasting, blood plasma glucose levels are
generally maintained within a range of 3.9-7.8mmol/L for healthy humans. Although 3.3 or 3.9mmol/L is
commonly cited as the lower limit of normal glucose, different values have been defined as low for different
populations, clinical purposes, or circumstances.
The precise level of glucose considered low enough to define hypoglycaemia is dependent on (1) the
measurement method, (2) the age of the person, (3) presence or absence of effects, and (4) the purpose of
the definition. While there is no disagreement as to the normal range of blood sugar, debate continues as to
what degree of hypoglycemia warrants medical evaluation or treatment, or can cause harm.
Method of measurement
Blood glucose levels are venous plasma or serum levels measured by standard, automated glucose oxidase
methods. For clinical purposes, plasma and serum levels are similar enough to be interchangeable. Arterial
plasma or serum levels are slightly higher than venous levels, and capillary levels are typically in between. This
difference between arterial and venous levels is small in the fasting state but is amplified and can be greater
than 10% in the postprandial state.
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On the other hand, whole blood glucose levels (e.g., by fingerprick meters) are about 10%-15% lower than
venous plasma levels. Furthermore, available fingerstick glucose meters are only warranted to be accurate to
within 15% of a simultaneous laboratory value under optimal conditions, and home use in the investigation of
hypoglycaemia is fraught with misleading low numbers. In other words, a meter glucose reading of 2.16mmol/L
could be properly obtained from a person whose laboratory serum glucose was 2.94mmol/l, even wider
variations can occur with "real world" home use. Ironically, most meters sold are routinely tested for
accuracy at the high-end of the scale, sometimes up to 44.4mmol/L, despite the fact that there is little
immediate danger from hyperglycaemia, whereas there is very real immediate danger from hypoglycaemia,
making accuracy at the low-end extremely critical.
Two other factors significantly affect glucose measurement: in newborn infants - increased hematocrit and a
delay in measuring low glucose levels; or adults with polycythaemia. High neonatal hematocrits are particularly
likely to confound glucose measurement by meter. Second, unless the specimen is drawn into a fluoride tube
or processed immediately to separate the serum or plasma from the cells, the measurable glucose will be
gradually lowered by in vitro metabolism of the glucose at a rate of approximately 0.39mmol/L/hr, or even
more in the presence of leukocytosis.
Purpose of definition
Deciding whether blood glucose in the borderline range of 2.5-4.2 mmol/l represents clinically problematic
hypoglycaemia is not always simple. This leads people to use different "cutoff levels" of glucose in different
contexts and for different purposes.
Pathophysiology
Like most animal tissues, brain metabolism depends primarily on glucose for fuel in most circumstances. A
limited amount of glucose can be derived from glycogen stored in astrocytes, but it is consumed within
minutes. For most practical purposes, the brain is dependent on a continual supply of glucose diffusing from
the blood into the interstitial tissue within the central nervous system and into the neurons themselves.
Therefore, if the amount of glucose supplied by the blood falls, the brain is one of the first organs affected.
In most people, subtle reduction of mental efficiency can be observed when the glucose falls to 3.6mmol/L.
Impairment of action and judgment usually becomes obvious below 2.2mmol/L. Seizures may occur as the
glucose falls further. As blood glucose levels fall below 0.55 mmol/L, most neurons become electrically silent
and nonfunctional, resulting in coma.
These brain effects are collectively referred to as neuroglycopenia. The importance of an adequate supply of
glucose to the brain is apparent from the number of nervous, hormonal and metabolic responses to a falling
glucose level. Most of these are defensive or adaptive, tending to raise the blood sugar via glycogenolysis and
gluconeogenesis or provide alternative fuels. If the blood sugar level falls too low the liver converts stored
glycogen into glucose and releases it into the bloodstream, to prevent the person going into a diabetic coma,
for a short period of time.
Brief or mild hypoglycaemia produces no lasting effects on the brain, though it can temporarily alter brain
responses to additional hypoglycemia. Prolonged, severe hypoglycaemia can produce lasting damage of a wide
range. This can include impairment of cognitive function, motor control, or even consciousness. The likelihood
of permanent brain damage from any given instance of severe hypoglycaemia is difficult to estimate, and
depends on a multitude of factors such as age, recent blood and brain glucose experience, concurrent
problems such as hypoxia, and availability of alternative fuels. The vast majority of symptomatic
hypoglycaemic episodes result in no detectable permanent harm.
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Signs and symptoms
Hypoglycaemic symptoms and manifestations can be divided into those produced by the counter regulatory
hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic
effects produced by the reduced brain sugar.
Adrenergic manifestations
Shakiness, anxiety, nervousness, tremor
Palpitations, tachycardia
Sweating, feeling of warmth
Pallor, coldness, clamminess
Dilated pupils (mydriasis)
Feeling of numbness "pins and needles"
(parasthaesia) in the fingers
Glucagon manifestations
Hunger,
vomiting, abdominal discomfort
Headache
Neuroglycopenic manifestations
Abnormal mentation, impaired judgment
Nonspecific dysphoria, anxiety, moodiness, depression, crying
Negativism, irritability, belligerence, combativeness, rage
Personality change, emotional lability
Fatigue, weakness, apathy, lethargy, daydreaming, sleep
Confusion, amnesia, dizziness, delirium
Staring, "glassy" look, blurred vision, double vision
Automatic behavior, also known as automatism
Difficulty speaking, slurred speech
Ataxia, incoordination, sometimes mistaken for "drunkenness"
Focal or general motor deficit, paralysis, hemiparesis
Paresthesia, headache
Stupor, coma, abnormal breathing
Generalized or focal seizures
Treatment and prevention
Management of hypoglycaemia involves immediately raising the blood sugar to normal, determining the cause,
and taking measures to hopefully prevent future episodes.
Reversing acute hypoglycemia
The blood glucose can be raised to normal within minutes by taking (or receiving) 10-20 grams of
carbohydrate. It can be taken as food or drink if the person is conscious and able to swallow. This amount of
carbohydrate is contained in about 100-120 ml of orange, apple, or grape juice although fruit juices contain a
higher proportion of fructose which is more slowly metabolized than pure dextrose, alternatively, about 120150 ml of regular (non-diet) soda may also work, as will about one slice of bread, about 4 crackers, or about 1
serving of most starchy foods. Starch is quickly digested to glucose (unless the person is taking acarbose),
but adding fat or protein retards digestion. Symptoms should begin to improve within 5 minutes, though full
recovery may take 10-20 minutes. Overfeeding does not speed recovery and if the person has diabetes will
simply produce hyperglycemia afterwards.
If a person is suffering such severe effects of hypoglycaemia that they cannot (due to combativeness) or
should not (due to seizures or unconsciousness) be given anything by mouth, medical personnel can establish
an IV and give intravenous Dextrose, of varying concentrations depending on age. If an IV cannot be
established, the patient can be given 1 to 2 milligrams of Glucagon in an intramuscular injection.
References
1. Philip E. Cryer (1997). Hypoglycemia: pathophysiology, diagnosis, and treatment. Oxford [Oxfordshire]: Oxford
University Press. ISBN 0-19-511325-X. OCLC 36188385.
2. Koh TH, Eyre JA, Aynsley-Green A (1988). "Neonatal hypoglycaemia--the controversy regarding definition".
Arch. Dis. Child. 63 (11): 1386–8. PMID 3202648.
3. Vasudevan A Raghavan, MBBS, MD, MRCP, Assistant Professor, Department of Internal Medicine, Divisions of
Endocrinology, Diabetes and Metabolism and Cardiovascular Sciences, Ohio State.
Questions
1. Define the term Hypoglycaemia.
2. Discuss the method of measurement for glucose.
3. Discuss the pathophysiology of hypoglycaemia including signs and symptoms.
Thistle QA is a SANAS accredited organisation, No: PTS0001
Accredited to ISO guide 43 and ILAC G13
Certificate available on request or at www.sanas.co.za